12 results about "Decitabine" patented technology

The invention belongs to the technical field of biological medicines, and discloses application of decitabine or an optical isomer thereof, or a hydrate thereof, or a solvate thereof, or a prodrug thereof, or a derivative thereof, or a pharmaceutically acceptable salt thereof in preparation of medicines for preventing and / or treating nasopharynx cancer. Or application in preparation of drugs for inhibiting postoperative recurrence and growth of nasopharyngeal carcinoma. In-vivo and in-vitro experiments prove that decitabine has the activity of remarkably inhibiting growth of nasopharyngeal carcinoma cells and is efficient and low in toxicity; the in-situ gel is prepared into the in-situ gel and is locally administrated through the nasopharyngeal cavity, so that toxic and side effects caused by a conventional treatment method can be avoided, tumor recurrence and growth can be remarkably inhibited after nasopharyngeal carcinoma operation, good safety is achieved, a new medicine and a new means are provided for prevention and treatment of nasopharyngeal carcinoma, and therefore the in-situ gel has wide application prospects.

The present invention provides a composition comprising a cytidine analog, in particular decitabine or azacitidine. In particular, the present invention provides a composition comprising a cytidine analog, in particular decitabine or azacitidine, which is useful for topical application. The present invention also provides the use of such compositions for medical conditions in the keratinizing and non-keratinizing epithelium / skin, such as the treatment of human papillomavirus (HPV)-related pre-cancerous conditions.

Disclosed herein include methods, compositions, and kits suitable for use in treating a hematological cancer in a subject. In some embodiments, the method comprises determining the presence or absence of at least one mutation in one or more genes encoding a spliceosome protein in sample nucleic acids from the subject; and administering onvansertib and decitabine to the subject, if the at least one mutation in one or more genes encoding a spliceosome protein is determined to be present in the sample nucleic acids, thereby reducing or inhibiting progression of the hematological cancer in the subject.

The invention discloses application of decitabine in preparation of a medicine for preventing and treating African swine fever. The research finds that decitabine has obvious anti-African swine fever virus activity and dose dependence, and can effectively inhibit expression of p30 protein and B646L gene of the African swine fever virus, so that the decitabine has a protective effect on cells infected with the African swine fever virus. The invention provides a new drug choice for resisting African swine fever virus infection, and has a wide application prospect in prevention and treatment of African swine fever.

The invention relates to application of a combination of decitabine and an anti-HER2 antibody in preparation of a medicine for treating tumors. The invention provides application of decitabine or an analogue thereof in preparation of a medicine for treating tumors in combination with an anti-HER2 (Human Epidermal Growth Factor Receptor 2) antibody. The invention also provides application of decitabine or an analogue thereof, an anti-HER2 antibody and one, more or all of a cell aging induction medicine, a ZBP1 agonist and an SETDB1 inhibitor in preparation of medicines for treating tumors. The present invention also provides pharmaceutical compositions and kits comprising decitabine or an analog thereof and an anti-HER2 antibody.

This invention discloses the application of the combined use of tanshinone and decitabine in the preparation of drugs for treating breast cancer, belonging to the field of antitumor drug application technology. This invention reveals a novel mechanism by which the combined use of tanshinone (Miltirone) and decitabine (DAC) inhibits breast cancer development by inducing pyroptosis and inhibiting epithelial-mesenchymal transition (EMT). Experimental verification shows that the combined treatment of Miltirone and DAC significantly reduces the viability of 4T1 breast cancer cells, inhibiting their proliferation, migration, and invasion abilities; simultaneously, this combined regimen induces significant pyroptosis by promoting the cleavage of pyroptosis-related proteins such as GSDME, accompanied by an increase in the release of LDH and ATP. This invention provides important experimental evidence and new ideas for the development of combination therapy strategies for breast cancer and the preparation of highly effective pyroptosis-inducing antitumor drugs.

Provided according to embodiments of the invention are methods of treating a disorder in a subject in need thereof that include administering to the subject an effective amount of cedazuridine, an effective amount of decitabine, and an effective amount of venetoclax, thereby treating the disorder in the subject. In some embodiments of the invention, the disorder is a hyperproliferative disorder such as a cancer. In some embodiments, the disorder is a hematological cancer such as myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), leukemia (e.g., acute myeloid leukemia), or lymphoma.

The invention relates to the use of AT7867, MC1568, ACY-1215, AZD-4547, NPK76- II-72-1, tivozanib, SAR-245409, HG-9-91-01, BIX-01294, UNC-669, WZ-7043, dacomitinib, CC-401, UNC-0638, epigallocatechin gallate (-), SB-239063, GDC-0879, KIN001-260, quizartinib, CGK-733, UNC-1215, XMD11-85H, garcinol, PF-573228, veliparib, VE-821, NVP-TAE684, GSK-J2, masitinib, KU-55933, KIN001-127, KIN001- 270, vandetanib, CG-930, GNF-2, decitabine, SGI-1776, amuvatinib, BS-181, CTB, MGCD-265, olaparib, ZM-447439, AGK-2, bosutinib, JNJ-38877605, RG-108, SYK- inhibitor, AZ-20, and OSI-930 drugs, which aim to suppress immune system escape mechanisms in cancer treatment and reduce the proliferation and survival abilities of cancer cells by interacting with proteins involved in immune escape processes and / or neighbouring proteins of these proteins, in T-cell-based immunotherapies.

Provided herein are compositions, systems, kits, and methods for treating a patient with cancer by alternate administration of decitabine and 5-azacytidine, or administration of decitabine two times per week on consecutive days, which is generally timed to bypass auto-dampening and exploit cross-priming. Such administration is combined with an inhibitor of the enzyme cytidine deaminase (e.g., tetrahydrouridine) that otherwise rapidly catabolizes decitabine and 5-azacytidine. In certain embodiments, the time between cycles of decitabine and 5-azacytidine administration is about three to four days or five to ten days.

The invention relates to the technical field of medicines, and provides application of zalcitabine in drugs for inhibiting and / or preventing and / or relieving and / or treating multiple myeloma in order to solve the problems that whether zalcitabine has anti-tumor activity in MM and related molecular mechanisms are not clear at present. The invention relates to a pharmaceutical preparation for inhibiting and / or preventing and / or relieving and / or treating multiple myeloma. The pharmaceutical preparation comprises an active ingredient and a pharmaceutically acceptable excipient, wherein the active ingredient is 2 ', 3'-dideoxycytidine. Researches show that zalcitabine induces mitochondrial dysfunction by targeted inhibition of expression of TFAM, and induces occurrence of ferroptosis of MM cells by triggering a cGAS-STING pathway through mtDNA cytoplasm stress. In-vivo animal experiments further show that zalcitabine can significantly slow down tumor growth. In addition, the antineoplastic activity of zalcitabine is also verified in a bone marrow sample derived from an MM patient.

Provided herein are compositions, systems, kits, and methods for treating a patient with cancer by alternate administration of decitabine and 5-azacytidine, or administration of decitabine two times per week on consecutive days, which is generally timed to bypass auto-dampening and exploit cross-priming. Such administration is combined with an inhibitor of the enzyme cytidine deaminase (e.g., tetrahydrouridine) that otherwise rapidly catabolizes decitabine and 5-azacytidine. In certain embodiments, the time between cycles of decitabine and 5-azacytidine administration is about three to four days or five to ten days.